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MBB164 - Molecular Biology > Dr Bird > Flashcards

Dr Bird Flashcards

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1
Q

How do most tumours develop?

A

Develop in epithelium, then metastasise into the mesenchyme and then into the muscle

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2
Q

What are the properties of benign tumours?

A
  • Develop in any tissue
    • Grow locally
    • May cause problems by pressure on brain or colon obstruction
      - Histologically resemble the tissue of origin
      - Do not spread to distant sites
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3
Q

What are the properties of in situ tumours?

A
  • Usually develop in the epithelium
    • Have altered histological appearance
    • Variations in cell size and shape
      - Do not invade basement membrane and supporting mesenchyme
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4
Q

What are the properties of cancers?

A
  • Fully developed malignant tumours with the specific capacity to invade and destroy the underlying mesenchyme
    - Metastasise
    - Stimulate angiogenesis and development of blood supply
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5
Q

What does the ability to metastasise mean?

A

Can spread to other tissues

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6
Q

What are the exogenous agents that can cause mutations in DNA?

A
  • Ionising radiation
    • UV radiation
    • Chemical carcinogens
    • Viruses
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7
Q

What are the endogenous agents that can cause mutations in DNA?

A
  • Errors in DNA replication
    • Intrinsic instability
    • Attack by free radicals
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8
Q

What is a transient mutation?

A

A mutation in DNA that can be repaired

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9
Q

How do tumours arise from mutations in DNA?

A

Permanent mutation occurs and cell division causes a tumour

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10
Q

What are the two broad classes of genes involved in the onset of cancer?

A

Proto-oncogenes and tumour suppressor genes

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11
Q

How are proto-oncogenes involved in the onset of cancer?

A

Excessively active in growth promotion

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12
Q

How are tumour suppressor genes?

A

Normally restrain cell growth but damage to these genes allows inappropriate growth

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13
Q

What is the effect of a point mutation?

A

Amino acid substitution

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14
Q

What is the effect of a frameshift mutation?

A

Scrambled sequence and truncated protein

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15
Q

What is the effect of a inappropriate expression or amplification mutation?

A

Normal protein at the wrong time or too much produced

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16
Q

What is the effect of a loss of gene mutation?

A

Loss of protein

17
Q

What is the effect of a fusion with another gene mutation?

A

Chimeric protein with altered funtion

18
Q

What is the effect of a epigenetic modification mutation?

A

Gene silencing and no protein

19
Q

What is the effect of breakage of bonds between purine and deoxyribose?

A

Random base insertions

20
Q

What is the effect of deamination of cytosine to uridine?

A

C -> U

21
Q

What is the effect of deamination of methylcytosine to thymidine?

A

C -> T

22
Q

What is the effect of ionising radiation on DNA?

A

Single and double stranded DNA breaks and damage from free radicals

23
Q

What is the effect of UV radiation on DNA?

A

Thymidine dimers

24
Q

What is the function of the p53 gene?

A

Surveys DNA for damage and elicits a repair

25
Q

How is DNA damage caused by thymidine dimers repaired?

A

Removal of whole stretch of DNA and resynthesis using opposite strand as template

26
Q

How is DNA damage caused by O-6 methyl guanine repaired?

A

Directly removed without breaking phosphate backbone

27
Q

How is DNA damage caused by single strand breaks repaired?

A

Directly repaired

28
Q

How is DNA damage caused by double strand breaks repaired?

A

Not easily repairable

29
Q

What are the necessary properties for a tumour to spread?

A
  • Self-sufficiency in growth signals
    - Insensitivity to antigrowth signals
    - Evasion of apoptosis
    - Limitless replicative potential
    - Tissue invasion and metastasis
    - Sustained angiogenesis
30
Q

What are growth signals generated by?

A
  • Diffusible growth factors
    • Extracellular matrix components
    • Cell to cell adhesion molecules
31
Q

What are examples of diffusible growth factors?

A
  • EGF (Epidermal growth factor)
    • FGF (Fibroblast growth factor)
    • TGFa (Transforming growth factor alpha)
    • PDGF (Platelet-derived growth factor)
32
Q

What are the three ways in which cancer cells become growth signal autonomous?

A
  • Modulation of growth factor provision
    • Modulation of growth factor receptor activity
    • Modulation of intracellular signalling pathways
33
Q

What is the method of growth factor signalling?

A
  • Growth factor binds to the receptor
    • Receptor becomes active as a tyrosine kinase and autophosphorylates on tyrosine residues
    • Some proteins can then dock with the receptor and become activated, others act as substrates for the receptor kinase and become phosphorylated (Usually protein kinases)
      - Phosphorylated protein then activates a transcription factor
34
Q

How does modulation of growth factor receptor activity cause cancer cells self sufficiency in growth signals?

A

Overexpression of the growth factor allows tumours to respond to low levels of growth factor that would not normally produce a growth response

MBB164 - Molecular Biology (4 decks)

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